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NFIB/MLL1 complex is required for the stemness and the Dlx5-dependent osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE227538 | GEO | 2023/09/05

REPOSITORIES: GEO

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NFIB/MLL1 complex is required for the stemness and the Dlx5-dependent osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:NFIB/MLL1 complex is required for the stemness and the Dlx5-dependent osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

| PRJNA945466 | ENA

Histone demethylase KDM4D cooperates with NFIB and MLL1 complex to regulate adipogenic differentiation of C3H10T1/2 mesenchymal stem cells.

Project description:The coordinated and sequential actions of lineage-specific transcription factors and epigenetic regulators are essential for the initiation and maintenance of cellular differentiation. We here report KDM4D histone demethylase as a key regulator of adipogenesis in C3H10T1/2 mesenchymal stem cells. The depletion of KDM4D results in impaired differentiation, which can be rescued by exogenous KDM4D, PPAR?, and C/EBP?, but not by C/EBP?. In addition, KDM4D interacts physically and functionally with both NFIB and MLL1 complex to regulate C/EBP? and PPAR? expression upon adipogenic hormonal induction. Although KDM4D is dispensable for the binding of both NFIB and MLL1 complex to the target promoters, the demethylation of tri-methylated H3K9 by KDM4D is required for NFIB and MLL1 complex to deposit tri-methylated H3K4 and activate PPAR? and C/EBP? expression. Taken together, our data provide a molecular framework for lineage-specific transcription factor and histone modifiers to cooperate in adipogenic differentiation, in which KDM4D removes repressive histone marks at genes with a bivalent chromatin domain and allows NFIB and MLL1 complex to promote the expression of key adipogenic regulators.

| S-EPMC7033117 | biostudies-literature

Genome-wide map of NFIB/MLL1 complex binding and H3K4me3 deposition during osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:To explore direct targets of NFIB/MLL1 complex and to examine the role of NFIB/MLL1 complex in genome-wide deposition of histone H3-K4 tri-methylation (H3K4me3), we conducted chromatin immunoprecipitation (ChIP) followed by deep sequencing (ChIP-seq) analysis of six different samples at two time points.

2023-09-05 | GSE227536 | GEO

The transcriptome analysis of C3H10T1/2 mesenchymal stem cells its derivatives expressing shRNA against NFIB or MLL1 during osteogenic differentiation

Project description:To examine the impact of the NFIB/MLL1 complex on the transcriptome of C3H10T1/2 mesenchymal stem cells (MSCs) and to identify NFIB/MLL1-dependent genes during osteogenic differentiation, we performed RNA-sequencing (RNA-seq) analysis of six different samples at two time points.

2023-09-05 | GSE227537 | GEO

Genome-wide map of NFIB/MLL1 complex binding and H3K4me3 deposition during osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:Genome-wide map of NFIB/MLL1 complex binding and H3K4me3 deposition during osteogenic differentiation of C3H10T1/2 mesenchymal stem cells

| PRJNA945468 | ENA

Effect of depletion of KDM4D, NFIB, and MLL1 on gene expression during adipogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:To investigate the cooperative function KDM4D/NFIB/MLL1 complex in the regulation of adipogenic differentiation, we established 10T1/2 cell lines in which each target gene has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.

2020-02-26 | GSE131369 | GEO

Effect of depletion of KDM4D, NFIB, and MLL1 on gene expression during adipogenic differentiation of C3H10T1/2 mesenchymal stem cells

Project description:The limited efficacy of currently approved immunotherapies in EGFR-mutant lung adenocarcinoma (LUAD) underscores the need to better understand alternative mechanisms governing local immunosuppression to fuel novel therapies. Elevated surfactant and GM-CSF secretion from the transformed epithelium induces tumor-associated alveolar macrophages (TA-AM) to proliferate and support tumor growth by rewiring inflammatory functions and lipid metabolism. TA-AM properties are driven by increased GM-CSF—PPARγ signaling and inhibition of airway GM-CSF or PPARγ in TA-AMs suppresses cholesterol efflux to tumor cells, which impairs EGFR phosphorylation and restrains LUAD progression. In the absence of TA-AM metabolic support, LUAD cells compensate by increasing cholesterol synthesis, and blocking PPARγ in TA-AMs simultaneous with statin therapy further suppresses tumor progression and increases T cell effector functions. These results reveal new therapeutic combinations for immunotherapy resistant EGFR-mutant LUADs and demonstrate how such cancer cells can metabolically co-opt TA-AMs through GM-CSF—PPARγ signaling to provide nutrients that promote oncogenic signaling and growth.

2024-04-25 | GSE249658 | GEO

The epigenetic regulator Mll1 is required for Wnt-driven intestinal tumorigenesis and cancer stemness.

Project description:Wnt/?-catenin signaling is crucial for intestinal carcinogenesis and the maintenance of intestinal cancer stem cells. Here we identify the histone methyltransferase Mll1 as a regulator of Wnt-driven intestinal cancer. Mll1 is highly expressed in Lgr5+ stem cells and human colon carcinomas with increased nuclear ?-catenin. High levels of MLL1 are associated with poor survival of colon cancer patients. The genetic ablation of Mll1 in mice prevents Wnt/?-catenin-driven adenoma formation from Lgr5+ intestinal stem cells. Ablation of Mll1 decreases the self-renewal of human colon cancer spheres and halts tumor growth of xenografts. Mll1 controls the expression of stem cell genes including the Wnt/?-catenin target gene Lgr5. Upon the loss of Mll1, histone methylation at the stem cell promoters switches from activating H3K4 tri-methylation to repressive H3K27 tri-methylation, indicating that Mll1 sustains stem cell gene expression by antagonizing gene silencing through polycomb repressive complex 2 (PRC2)-mediated H3K27 tri-methylation. Transcriptome profiling of Wnt-mutated intestinal tumor-initiating cells reveals that Mll1 regulates Gata4/6 transcription factors, known to sustain cancer stemness and to control goblet cell differentiation. Our results demonstrate that Mll1 is an essential epigenetic regulator of Wnt/?-catenin-induced intestinal tumorigenesis and cancer stemness.

| S-EPMC7752919 | biostudies-literature

The transcriptome analysis of C3H10T1/2 mesenchymal stem cells its derivatives expressing shRNA against NFIB or MLL1 during osteogenic differentiation

Project description:The transcriptome analysis of C3H10T1/2 mesenchymal stem cells its derivatives expressing shRNA against NFIB or MLL1 during osteogenic differentiation

| PRJNA945472 | ENA

TAZ promotes osteogenic differentiation of mesenchymal stem cells line C3H10T1/2, murine multi-lineage cells lines C2C12, and MEFs induced by BMP9.

Project description:Bone morphogenetic protein 9 (BMP9), also named as growth differentiation factor 2 (GDF-2), is the strongest cytokine that promotes osteogenic differentiation in the BMP family, and has broad clinical application value. Nevertheless, the mechanism of BMP9 promotes osteogenic differentiation remain unclear. TAZ, a transcriptional co-activator, has great effects on cell proliferation, differentiation, and stem cell self-renewal. In this research, we investigated the effects of TAZ in BMP9-induced osteogenic differentiation of mesenchymal stem cell line C3H10T1/2 (MSCs) and murine multi-lineage cell lines C2C12 and MEFs (MMCs) and explored its possible mechanisms. This study has found that BMP9 induces the expression of TAZ and promotes its nuclear translocation. Meanwhile, our study found that Ad-TAZ and TM-25659, a TAZ agonist, can enhance the osteogenic differentiation of MSCs and MMCs induced by BMP9. Conversely, Ad-si-TAZ and verteporfin, an inhibitor of TAZ, have the contradictory effect. Likewise, the promotion of TAZ to the BMP9-induced ectopic bone formation in vivo was confirmed by the subcutaneous transplantation of MSCs in nude mice. Furthermore, we have detected that TAZ might increase the levels of the phosphorylation of Smad1/5/8, p38, ERK1/2, and JNK induced by BMP9. Additionally, we also found that TAZ increased the total protein level of β-catenin induced by BMP9. In summary, our results strongly indicated that TAZ will promote the osteogenic differentiation in MSCs and MMCs induced by BMP9 through multiple signal pathways.

| S-EPMC9794779 | biostudies-literature

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